Renal 2- acute kidney injury and nephritic/ nephrotic syndrome Flashcards
Definition of AKI
A rapid (within hours to days) fall in glomerular filtration rate which impedes the kidney’s normal functions
AKI stage 1
Increase in serum cratinine of 26 micromol/ litre or more within 48 hours
OR
1.5-2x increase from baseline
Less than 0.5ml/kg/hour for more than 6 hours
AKI stage 2
Increase in serum creatinine to more than 2-3x from baseline
Less than 0.5ml/kg/hour for more than 12 hours
AKI stage 3
Increase in serum creatinine to more than 3x from baseline
OR
Serum creatinine more than 354 micromol/litre with an acute increase of at least 44 micromol/litre
Less than 0.3ml/kg/hour for 24 hours or anuria for 12 hours
What is creatinine?
A normal product of muscle turnover
Non-toxic
Transported by the blood and excreted by the kidneys
Used as a surrogate marker for glomerular filtration
Less filtration -> less creatinine removed -> a creatinine rise
GFR is estimated from creatinine results
Normal range of creatinie
In Brighton 60-100 micromols/litre
What is normal for one patient may not be for another
Oliguria
<0.5ml/kg/hour urine output
Usually <500ml/ 24 hours in adults
Anuria
Officially would mean no urine output
Softly defined as <100ml/ 24 hours
Four phases of AKI
Onset phase
Oliguric/ anuric phase
Polyuric/ diuretic phase
Recovery phase
Onset phase- hours to days
Common triggering events
- significant blood loss
- burns
- fluid loss
- diabetes insipidus
Renal blood flow 25% of normal
Tissue oxygenation 35% pf normal
Urine output below 0.5ml/kg/hour
Oliguric/ anuric phase- 8-14 days or longer depending on nature of AKI
Urine output below 400ml/day, possibly as low as 100ml/day
Increase in BUN and creatinine levels
Electrolyte disturbances, acidosis and fluid overload (from kidney’s inability to excrete water)
Diuretic phase- 7-14 days
Occurs when AKI is corrected
Renal tubule scarring and oedema
Increased GFR
Daily urine output above 400ml
Possible electrolyte depletion from excretion of more water and osmotic effects of high BUN
Recovery phase- several months to 1 year
Decreased oedema
Normalisation of fluid and electrolyte balance
Return of GFR to 70% or 80% of normal
Kidney functions
Excretion of toxins
Electrolyte balance
Acid base balance
Fluid balance
NP control
Control of bone metabolism, vit D activation, phosphate excretion
Production of erythropoietin
Hyperkalaemia
K+ >6.0 = bad
K+ >6.5 = medical emergency
ECG
- reduced P wave with widened QRS
- tented T waves
- sine wave pattern
Fluid overload
Symptoms
- breathlessness
- orthopnoea
- limb swelling
The danger- pulmonary oedema- severe tissue hypoxia
If patient is oliguric/ anuric they won’t be able to get rid of excess water
When to think about dialysis
- Refractory hyperkalaemia
- Pulmonary oedema
- Refractory acid/ base disturbance
- Uraemic complications (coma, pericarditis)
What causes AKI?
- Pre-renal causes
- Renal causes
- Post-renal causes
Pre-renal causes
Decrease in perfusion pressure resulting in ischaemia or infarction
- bleeding
- septic shock
- dehydration
- myocardial infarction
- iatrogenic
- renal artery stenosis
VERY LIKELY
Renal causes
Direct toxic effects
- drugs
- calcium and other metals
Overproduction leading to blockage of the tubules
- rhabdomyolysis
- myeloma
Inflammation in the kidney
- GN
- interstitial nephritis
- ATN
UNLIKELY
Post renal causes
Plumbing problem/ outflow obstruction
- stones
- ureteric/ urethral strictures
- BPH
- prostate cancer
- urinary retention e.g. neurogenic, constipation
Relatively LIKELY
Who is at risk of AKI?
Chronic background risk:
- elderly
- CKD
- cardiac failure
- liver disease
- diabetes
- vascular disease
- background nephrotoxic medications
Acute risk:
- S: sepsis and hypoperfusion
- T: toxins
- O: obstruction
- P: parenchyma
Predict/ prevent AKI- the 4 Ms
Monitor
- obs/NEWS, regular blood tests, fluid balance charts, pathology alerts
Maintain circulation
- hydration, resuscitation, oxygenation
Minimise kidney insults
- nephrotoxic meds, surgery, contrast, hospital acquired infection
Mange the acute illness
- sepsis, heart failure, liver failure
Treatment of AKI
Make the patient safe
- ABCDE
- what is K+
- what is volume status
If hypovolaemic give 250/500ml bolus of saline
Monitoring
- check catheter
- strict fluid inputs/ outputs
- check VBG
Investigate the cause once stable
Red flags in history
Haemoptysis
Rashes
Joint pain/ swelling
ENT- crusting of nose/ acute hearing impairment
Significant acute limb swelling
Noticeable urine frothiness
Jaundice
Drugs to hold in AKI
ACE inhibitors
Angiotensin receptor blockers
NSAIDS: ibuprofen, diclofenac, naproxen
Any diuretics
Metformin
Causes of polyuria
Known and common phase of AKI of any cause
Post relief of obstruction
Diabetes mellitus
Psychogenic
Beer potomania
Rare endocrine causes (e.g. diabetes insipidus)
Managing polyuria
Encourage the patient to drink
Depending on your assessment of fluid balance
- provide IV fluids to match the output +/- additional input if dry
- once renal function begins to improve reduce to 75% of urine output
Managing oliguria
Depending on your assessment of fluid balance
If you have given 2-3 litres and can’t see blood on the floor ask for help
